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A study just published in the New England Journal of Medicine points to the value of conducting a new series of Alzheimer's prevention studies, suggests Cure Alzheimer's Consortium member Sam Gandy in an accompanying NEJM editorial. The study, led by Washington University's Randall J. Bateman, found that patients with a more genetic-oriented form of Alzheimer's experience a rise in beta-amyloid (Aβ) up to 25 years before symptoms begin -- and an increased level of tau protein up to 15 years before symptoms.

On Friday, August 24, Eli Lilly announced that their beta-amyloid immunotherapy (solanezumab) failed to meet its primary clinical endpoints for Alzheimer's disease. This disappointment follows the recent failure of another promising beta-amyloid immunotherapy, bapineuzumab from Pfizer/Johnson and Johnson-Jannsen/Elan. Both drugs failed in Phase 3 clinical trials, where they were being tested for their actual effect on Alzheimer's patients.

The David K. Johnson (DKJ) Foundation was created in 2000 in honor and memory of David and Susan Johnson of Reading, Mass., to promote awareness of and provide support for individuals and families affected by Alzheimer’s disease.

A new study of an existing drug for immune disorders that may have positive effects for Alzheimer’s patients has attracted national attention lately. While phase III clinical trial results for Gammagard, an IVIG or “intravenous immunoglobulin therapy” by Baxter International are not expected until early 2013, hope for success must be balanced with a hard look at the data. The Wall Street Journal’s story on this drug and the prognosis for success by Dr.

It was announced yesterday that Bapineuzumab, the Abeta immunotherapy drug, failed to meet cognitive and functional goals in a late stage trial of Alzheimer's patients who carry the APOE4 variant. “There was no reason to believe, unless there was a miracle, that this would be positive. It will only be the results of the non-APOE4 carriers that will inform us about the future [of bapineuzumab].” said Rudolph Tanzi, Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School and MGH in Boston and Chair of the Cure Alzheimer’s Research Consortium.

Cure Alzheimer’s Fund is pleased to salute Massachusetts General Hospital for placing number 1 in the current issue of U.S. News and World Report’s “Best Hospital” survey. While Cure Alzheimer’s Fund has supported more than 24 leading Alzheimer’s research institutions since its inception in 2004, Mass General has received almost $10 million in research grants from Cure Alzheimer’s Fund during that time.

Genes are the specific DNA blueprints for life, and all genes play roles that are essential for health. But some can carry DNA variants that influence risk for disease, either by increasing or decreasing susceptibility. If a variation in a gene is very rare, it’s called a mutation. The mutation may cause disease, increase risk for a disease, protect against a disease, or have no impact on health at all.

The New York Times Magazine appearing on Sunday, June 10, 2012, and available now online, carries a powerful narrative of a family’s journey through the tragedy of early-onset Alzheimer’s. It is a great contribution to Alzheimer’s awareness and the need for more research to end this disease, and a reinforcement of the priorities that the director of the National Institutes of Health has put on genetic research into the origins of Alzheimer’s.

Dr. Cathy Greenblat hasn’t always been a photographer, but she has always followed her heart. Before taking early retirement from Rutgers University, where she was a sociology professor for 35 years, she took a sabbatical in the spring of 2001 and made a decision that ultimately would change her life.

Alzheimer’s research for many years has been dominated by a focus on Abeta “plaques,” a focus that largely has overlooked the other infamous hallmark of the disease—the tau-based neurofibrillary “tangles.” The research world recently has broadened its scope to include significant research into tau.